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D. Dejour, P.G. Ntagiopoulos

170

Trochlear dysplasia (roots from the Greek

words

“dys-”

: mal- and

“plasis”:

creation

[13]) is a developmental condition in which the

femoral trochlea lacks of its normal and

sophisticated concave anatomy, that is

absolutely necessary to engage the patella, and

instead, it becomes shallow, flat or even convex.

According to A. Amis [14], who published the

first biomechanical results on patellar instability

in trochlear dysplasia and the efficacy of

trochleoplasty procedures, it is recognized that

the mediolateral flattening of the anterior

surface of the trochlear facets results

predominantly from an

excess of bone centrally

in the groove

. In its major pattern it forms a

supratrochlear prominence or “bump” anterior

to the shaft of the femur, which the patella has

to override when the knee starts to flex in order

to engage in the groove for the remaining

degrees of flexion. Amis

et al.

showed that

simulated trochlear dysplasia led to significant

reduction in lateral stability and that by re-

creating a deep trochlear groove with a

deepening trochleoplasty procedure, lateral

stability increased significantly similarly to the

intact knee [14].

The genetic and primitive origin of trochlear

dysplasia and its familiar occurrence have

been shown by C. Tardieu and J.L. Jouve.

There is evidence that the asymmetrical

trochlear shape in adults exists in the foetus

since the third trimester of pregnancy,

something that could prove the genetic roots of

trochlear dysplasia [15, 16]. The shape of the

articular trochlea is variable in mammals

depending on their type of locomotion:

unguligrade, digitigrade or plantigrade [17].

The asymmetrical ingression of the patella into

the normal trochlea is a characteristic of the

modern man. Christine Tardieu’s extensive

anthropomorphometric studies on this field

have showed that the femoral valgus angle, the

femoral bicondylar angle and the morphology

of the normal trochlea and its articulation with

the patella are not present in prime mammals

or non-walking children and are the result of

human erect stance and bipedalism [17-19].

These anatomic characteristics of the trochlea

could have been integrated into the genome

during the course of evolution [17, 20].

According to Tardieu, the oblique angle of the

femur is the major feature, which initiated the

later modifications of the patellofemoral joint

that over 3 million years before, were never

inscribed in the human genome. The elevated

lateral femoral facet and the deep trochlear

groove are features that

“were first acquired,

then once selected, genetically assimilated,

and now appear on the foetal cartilaginous

epiphysis”

[17].

It is surprising that the origin of the study on

the abnormal trochlear shape in patellar

dislocation starts more than 200 years ago in

Europe. Although the term ‘dysplasia’ was not

originally used, the earliest reference on this

condition can be attributed to Richerand in

1802. According to Isermeyer [21], Richerand

made the very first description of the abnormal

morphology of the trochlear groove and the

lateral femoral facet in paediatric patients with

patellar dislocation. The interest on the

abnormal trochlear shape in (mainly)

congenital patellar dislocation is also

documented in the works of B. Pollard in 1891

[22] and D. Drew in 1908 [23], who focused

on the effects of a

“possibly congenital”

reduced lateral facet height on improper

patellar engagement and lateral patellar

dislocation, and even attempted to surgically

create a new groove for the patella. According

to S. Donell and C. Hing [24], in 1914, J.

Murphy also considered the shallow trochlear

groove as a cause for patellar dislocation, and

he performed a similar surgical correction by

burring the groove and adding fat tissue

between the patella and the femur to reduce

scarring and adhesions by the exposed

cancellous bone [25]. The next year, in 1915,

Fred H. Albee from the

“New York

Postgraduate Medical School Clinic”

, was the

first who tried to surgically correct trochlear

dysplasia properly with his pioneer procedure:

the lateral facet elevating trochleoplasty

(fig. 1) [26]. This was a completely opposite

concept and it included adding a bone graft

under the lateral facet in order to augment the

required mechanical block for a pathological

lateral patellar translation. This procedure

gained, for a period of time, overseas attraction

mostly in the U.K. and less in France.